Q-omics provides the consensus-scored NFIB profile across patient tissues and cancer cell-line models. NFIB expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, NFIB is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, NFIB protein abundance shows 21,871 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where NFIB shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for NFIB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NFIB survival associations across molecular data types. NFIB RNA expression shows survival associations in the most cancer types (22), followed by mutation status (8) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NFIB RNA expression–survival associations across cancer types. High NFIB expression shows unfavorable associations in KICH, but favorable associations in KIRC, THCA, HNSC, LGG and PRAD. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for NFIB RNA expression.
This table summarizes NFIB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for NFIB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NFIB shows lower tumor expression in BLCA, LUSC, KICH, BRCA and LUAD and higher tumor expression in KIRC. The KIRC box plot shows higher NFIB RNA expression in tumor versus normal tissue (log2 FC = +0.802, t-test p < 0.001).
This table shows molecular features associated with NFIB in patient tissues and cancer cell lines. In patient samples, NFIB shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, NFIB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and SOFT_TISSUE.
